We propose a new hypothesis to explain the failure of mammalian retinal regeneration. The hypothesis suggests that maturing optic axons lose their adhesivity and therefore do not form fiber bundles, grow for long distances, or extend in the appropriate direction. We plan to restore this adhesivity by applying to the lesioned adult mouse retina a variety of selected pharmacologic agents. We also will attempt to disrupt normal axonal fasciculation and guidance in the embryonic chick retina by injecting into the eye specific lectins (carbohydrate-binding molecules). Positive results would suggest the involvement of cell-surface carbohydrates in the processes of axonal fasciculation and guidance.